ACP American College of Physicians - Internal Medicine - Doctors for Adults

Clinical Information

• PIER - Decision Support
• Guidelines
• Journals & Publications
• Additional Resources
  • Bedside Diagnosis
  • Bioterrorism
  • Lyme Disease Initiative
  • End of Life Care

Nerve Gases

General Characteristics

• Nerve gases include GA (Tabun), GB (Sarin), GD (Soman), VX, and GF
• Nerve gases are potent organophosphate compounds that inhibit acetylcholinesterease, causing a cholinergic crisis
• Many countries and terrorist groups have the capability to manufacture these or similar agents

Victim Triage

• Since all nerve agents are heavier than air they will sink:
• • The triage point should be upwind and uphill of the center of the event
  • Paramedics entering the zone of contamination must wear level A personal protective gear
• Victims must be hosed off with copious amounts of water
• Once decontaminated, victims should be medically evaluated for symptoms and the need to administer antidotes

Pathophysiology

• Nerve agents bind to acetylcholinesterase in a two-stage process:
• • The first stage is reversible with treatment pralidoxime
  • The second stage, or "aging," is irreversible
• Acetylcholinesterase breaks down the neurotransmitter acetylcholine:
• • Acetylcholine remains at its post-synaptic receptor sites causing excessive cholinergic stimulation
• Muscarinic stimulation produces the DUMBELS syndrome:
• • Diarrhea, urination, miosis, bradycardia and bronchorrhea, emesis, lacrimation, salivation
• Nicotinic receptor stimulation produces the MTWHF syndrome:
• • Muscle pain, tremors, weakness, hypertension, fasciculation
  • Symptoms can range from muscle weakness to profound paralysis
• Central nervous system effects:
• • Nerve agents freely cross the blood-brain barrier
  • Confusion, altered consciousness, seizures, and coma are possible symptoms

Treatment

• Counteract the cholinergic excess at all three receptor sites:
• • Atropine counteracts only muscarinic effects
  • Pralidoxime (protopam) counteracts the nicotinic effects
  • Benzodiazepines counteracts the CNS effects
• Muscarinic symptoms:
• • Localized ocular symptoms may be treated with anticholinergic eye drops (scopolamine or homatropine)
  • Isolated bronchospasm can be treated with ipratropium bromide
  • Hypersalivation, bronchial secretions, or bradycardia can be treated with large doses of intravenous atropine, titrated to clearing of the excess secretions (not bradycardia or pupil size)
• Nicotinic symptoms:
• • Pralidoxime (2-PAM) reactivates the enzyme acetylcholinesterase at the neuromuscular junction
  • It can only reactivate the enzyme if the aging process has not occurred, which varies from 5 minutes to 24 hours, depending upon the nerve agent
  • The recommended initial dose of 2-PAM is 1 to 2 grams I.V. slowly over 10 to 30 minutes
• Central nervous system symptoms:
• • Any of the intravenous benzodiazepines can be used to treat seizures
  • Phenytoin and fosphenytoin are not effective
• Patient monitoring:
• • Those with only minor symptoms, such as eye findings, may be watched for 6 to 8 hours and released if no further symptoms occur
  • Any patient who received 2-PAM should be hospitalized in an ICU
  • Any patient with neuromuscular weakness may require intubation and mechanical ventilation

Delayed Syndromes

• Intermediate syndrome:
• • Can occur within a few days of exposure, usually after some recovery has manifested itself
  • Symptoms include a new onset of descending paralysis, clinically similar botulism, and may require re-intubation and mechanical ventilation
• OPIND (organophosphate induced delayed neuropathy):
• • Caused by a slow inhibition of a second enzyme, NTE, up to a month after the initial exposure
  • Can lead to a sensory and motor distal neuropathy similar to Guillian-Barré syndrome
  • Recovery can be slow and incomplete

• Careers at ACP
• Contact Us
• Privacy Policy
• Site Map
• For Advertisers
• For Media
• For Governors
• For Regents